Fifteen one-piece cast frameworks simulating bars for fixed prosthesis in a model with five implants were fabricated and arranged into three different groups according to the material used for casting: CP Ti (commercially pure titanium), Co-Cr (cobalt-chromium) or Ni-Cr-Ti (nickel-chromium-titanium)
alloys. Each framework was installed over the metal model with all screws tightened to a 10 N cm torque and then, vertical misfits were measured using an optical microscope. The stresses selleck chemical transmitted to implants were measured using quantitative photoelastic analysis in values of maximum shear stress (T), when each framework was tightened to the photoelastic model to a 10 N cm standardized torque. Stress data were statistically analyzed using one-way ANOVA and Tukey’s test and correlation tests were performed
using Pearson’s rank correlation (alpha = 0.05). Mean and standard deviation values of vertical misfit are presented for CP Ti (22.40 +/- 9.05 mu m), Co-Cr (66.41 +/- 35.47 mu m) and Ni-Cr-Ti (32.20 +/- 24.47 mu m). Stresses generated by Co-Cr alloy (tau = 7.70 +/- 2.16 kPa) were significantly higher than those generated by CP Ti (tau = 5.86 +/- 1.55 kPa, click here p = 0.018) and Ni-Cr-Ti alloy (tau =5.74 +/- 3.05 kPa, p = 0.011), which were similar (p = 0.982). Correlations between vertical misfits and stresses around the implants were not significant as for any evaluated materials. (C) 2011 Elsevier Ltd. All rights reserved.”
“Tuberculosis, caused by Mycobacterium (M.) tuberculosis, is a devastating infectious disease causing many deaths worldwide. Non-specific host defense mechanisms such as the coagulation and fibrinolytic system may give insight in mTOR activity possible new therapeutic targets. Plasminogen activator inhibitor type-1 (PAI-1), an important regulator of inflammation and fibrinolysis, might be of interest as tuberculosis patients have elevated plasma levels of PAI-1. In this study we set out to investigate the role of PAI-1 during tuberculosis in vivo. Wildtype (WT) and PAI-1 deficient (PAI-1(-/-)) mice were intranasally infected with M. tuberculosis H37rv and sacrificed after 2,5 and 29 weeks. Five weeks post-infection, bacterial loads
in lungs of PAI-1(-/-) mice were significantly higher compared to WT mice, while no differences were seen 2 and 29 weeks post-infection. At two weeks post-infection increased influx of macrophages and lymphocytes was observed. PAI-1 deficiency was associated with a reduced cytokine response in the lungs; however, upon stimulation with tuberculin purified protein derivative (PPD), PAI-1(-/-) splenocytes released increased levels of IFN-gamma compared to WT. No clear differences were found between PAI-1(-/-) and WT mice at 29 weeks after infection. In conclusion, these data suggest that PAI-1 contributes to transient, non-specific changes in immunity during the early phase of murine tuberculosis. Crown Copyright (C) 2012 Published by Elsevier Masson SAS on behalf of Institut Pasteur.